Acquired hemophilia A in a patient with advanced prostate cancer.

Acquired hemophilia A (AHA) is a rare disorder that results from the presence of autoantibodies against the clotting factor VIII (FVIII) causing hemorrhagic disorders. This entity is mostly associated with autoimmune diseases, pregnancy, the postpartum period, drugs and malignancy. Among the solid cancers, prostate neoplasm is the most common cause of AHA. The management of AHA involves the control of active bleeding and the use of specific therapies to eliminate the inhibitor. The authors describe the case of an 87-year-old man with prostate cancer who developed a bleeding disorder 5 years after the cancer diagnosis. Treatment with prednisone did not reach a satisfactory clinical response, which was only achieved with the association of azathioprine. The patient became asymptomatic with no further bleeding episodes, but developed a fatal sepsis after 3 months of treatment with these immunosuppressive agents.

Plasmacytoid urothelial carcinoma: a case of histological variant of urinary bladder cancer with aggressive behavior.

Plasmocytoid variant urothelial carcinoma (PVUC) of the urinary bladder is a rare histological variant of transitional cell carcinoma. Data regarding PVUC shows that this neoplasia presents a distinctive clinical outcome represented by aggressive behavior and poor survival rate. The authors report a case of a 57-year-old male patient with a 3-month history of hematuria and pelvic pain. Radical cystectomy with lymphadenectomy was performed and pathological examination showed a pT3pN0 PVUC of the bladder. The patient remained free of recurrence for 8 months, but the disease recurred involving the abdominal wall and subcutaneous tissue. Chemotherapy provided a positive clinical response and relief of symptoms. The authors call attention to the aggressiveness of this rare variant of bladder cancer and recommend radical surgery and multidisciplinary management of this neoplasm.

Physicochemical characterization of metabolic acidosis induced by normal saline resuscitation of patients with severe sepsis and septic shock. / Caracterização físico-química da acidose metabólica induzida pela expansão volêmica inicial com solução salina a 0,9% em pacientes com sepse grave e choque séptico.

OBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9% saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE). RESULTS: Eight patients with a mean age of 58 ± 13 years and mean APACHE II scores of 20 ± 4 were expanded using 2,000 ± 370 mL of 0.9% saline solution. Blood pH dropped from 7.404 ± 0.080 to 7.367 ± 0.086 (p=0.018), and PC O2 increased from 30 ± 5 to 32 ± 2 mmHg (p=0.215); SBE dropped from -4.4 ± 5.6 to -6.0 ± 5.7 mEq/L (p=0.039). The drop in SBE was associated with the acidifying power of two factors, namely, a significant increase in the strong ion gap (SIG) from 6.1 ± 3.4 to 7.7 ± 4.0 mEq/L (p = 0.134) and a non-significant drop in the apparent inorganic strong ion differences (SIDai) from 40 ± 5 to 38 ± 4 mEq/L (p = 0.318). Conversely, the serum albumin levels decreased from 3.1 ± 1.0 to 2.6 ± 0.8 mEq/L (p = 0.003) with an alkalinizing effect on SBE. Increased serum chloride levels from 103 ± 10 to 106 ± 7 mEq/L (p < 0.001) led to a drop in SIDai. CONCLUSION: Initial resuscitation using 30 mL/kg of 0.9% saline solution for patients with severe sepsis and septic shock is associated with worsened metabolic acidosis, as measured by SBE. This worsened SBE can be ascribed to a serum increase in the levels of unmeasurable anions and chloride.

Caracterização físico-química da acidose metabólica induzida pela expansão volêmica inicial com solução salina a 0,9 por cento em pacientes com sepse grave e choque séptico / Physicochemical characterization of metabolic acidosis induced by normal saline resuscitation of patients with severe sepsis and septic shock

OBJETIVO: O objetivo deste estudo foi caracterizar e quantificar a acidose metabólica causada pela expansão volêmica inicial na reanimação de pacientes com sepse grave e choque séptico. MÉTODOS: Uma coleta de sangue para caracterização físico-química do equilíbrio ácido-básico antes e após a expansão volêmica com 30 mL/kg de solução salina a 0,9 por cento. O diagnóstico e a quantificação da acidose metabólica foram feitas com o uso do "standard base excess" (SBE). RESULTADOS: Oito pacientes com 58 ± 13 anos e APACHE II de 20 ± 4 foram expandidos com 2000 ± 370 mL de solução salina a 0,9 por cento. Houve queda do pH de 7,404 ± 0,080 para 7,367 ± 0,086 (P=0,018) associada a elevação da PCO2 de 30 ± 5 mmHg para 32 ± 2 mmHg (P=0,215) e queda do SBE de -4,4 ± 5,6 para -6,0 ± 5,7 mEq/L (P=0,039). Esta queda do SBE foi associada ao poder acidificante de dois fatores: elevação não significativa do "strong ion gap" (SIG) de 6,1 ± 3,4 para 7,7 ± 4,0 mEq/L (P=0,134) e queda não significativa do "strong ion diference" aparente inorgânico (SIDai) de 40 ± 5 para 38 ± 4 mEq/L (P=0,318). Em contraposição, houve queda da albumina sérica de 3,1 ± 1,0 para 2,6 ± 0,8 mEq/L (P=0,003), que teve um poder alcalinizante sobre o SBE. A elevação do cloro sérico de 103 ± 10 para 106 ± 7 mEq/L (P<0,001) gerou a queda do SIDai. CONCLUSÃO: A reanimação inicial de pacientes com sepse grave e choque séptico com 30 mL/Kg de solução salina a 0,9 por cento é associada a piora da acidose metabólica aferida pelo SBE. Esta piora do SBE pode ser atribuída a uma elevação dos ânions não mensuráveis e do cloro sérico.

OBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9 percent saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE). RESULTS: Eight patients with a mean age of 58 ± 13 years and mean APACHE II scores of 20 ± 4 were expanded using 2,000 ± 370 mL of 0.9 percent saline solution. Blood pH dropped from 7.404 ± 0.080 to 7.367 ± 0.086 (p=0.018), and PC O2 increased from 30 ± 5 to 32 ± 2 mmHg (p=0.215); SBE dropped from -4.4 ± 5.6 to -6.0 ± 5.7 mEq/L (p=0.039). The drop in SBE was associated with the acidifying power of two factors, namely, a significant increase in the strong ion gap (SIG) from 6.1 ± 3.4 to 7.7 ± 4.0 mEq/L (p = 0.134) and a non-significant drop in the apparent inorganic strong ion differences (SIDai) from 40 ± 5 to 38 ± 4 mEq/L (p = 0.318). Conversely, the serum albumin levels decreased from 3.1 ± 1.0 to 2.6 ± 0.8 mEq/L (p = 0.003) with an alkalinizing effect on SBE. Increased serum chloride levels from 103 ± 10 to 106 ± 7 mEq/L (p < 0.001) led to a drop in SIDai. CONCLUSION: Initial resuscitation using 30 mL/kg of 0.9 percent saline solution for patients with severe sepsis and septic shock is associated with worsened metabolic acidosis, as measured by SBE. This worsened SBE can be ascribed to a serum increase in the levels of unmeasurable anions and chloride.